Outbreak of Pharyngoconjunctival Fever at a Summer Camp --
North Carolina, 1991

On July 19, 1991, the Communicable Disease Section of the
North Carolina Department of Environment, Health, and Natural
Resources (DEHNR) was notified that an outbreak of acute upper
respiratory illness had occurred in campers and counselors at a
4-week summer camp. Manifestations of the illness included
pharyngitis, cough, fever to 104 F (40 C), headache, myalgia,
malaise, and conjunctivitis. On August 2, the DEHNR was notified of
a similar outbreak during a second 4-week session at the camp. The
epidemiologic investigation, initiated by the DEHNR on August 7,
identified the cause as pharyngoconjunctival fever (PCF) associated
with infection with adenovirus type 3. This report summarizes
findings from the investigation.

The first camp session (June 16-July 12) was attended by 768
boys aged 7-16 years and 300 counselors aged 17-22 years. On July
12, first-session campers returned home, but counselors remained at
the camp for the second session (July 14-August 9), which 800 boys
attended. Approximately 700 persons swam each day in a 1-acre,
manmade pond that had a maximum depth of 10 feet. Well water was
continuously pumped into the pond at multiple sites through pipes
located one foot below the surface of the water; the water
overflowed, through a spillway, into an adjacent river. An
automatic chlorination system treated the water before it entered
the pond. The pond water was turbid, and plants grew in the bottom
of the pond.

During the first session, 226 persons (175 campers and 51
staff members (i.e., counselors, administrative staff, and
infirmary personnel)) visited the camp infirmary because of onset
of symptoms of upper respiratory illness. During the second
session, 369 campers and 86 staff members visited the infirmary
with the same upper respiratory manifestations noted during the
first session.

A convenience sample of 181 campers from the second session
and 40 staff members at the camp was interviewed. A case of PCF was
defined as two of four symptoms -- sore throat, fever, cough, and
red eyes -- lasting more than 1 day. The attack rate for those
surveyed was 112 (52%) (88 campers (Figure 1) and 24 staff members)
of 216; duration of illness was unknown for five persons.

Every camper swam at least once during the 4 weeks; 158 (90%)
of 175 swam one or more times per day. The attack rate for campers
who swam daily (74 (48%) of 153) did not differ significantly from
that for campers who swam less than once per week (11 (65%) of 17
(relative risk (RR)=0.8; 95% confidence interval (CI)=0.5-1.3)).
The attack rate for staff who swam was higher than that for staff
who did not swim (10 (77%) of 13 versus 13 (54%) of 24 (RR=1.4; 95%
CI=0.9-2.3)) and increased with increased frequency of swimming.
The attack rate for nonswimmers was 54% (13 of 24); for infrequent
swimmers (i.e., those who swam once per week or less), was 75% (six
of eight); and for frequent swimmers (i.e., those who swam three or
more times per week), was 80% (four of five). Of the 221 campers
and staff members interviewed, 75 (41 campers and 34 staff members)
reported whether they had shared a towel with another person. Towel
sharing increased the risk for illness (11 of 12 who shared versus
31 of 63 who did not (RR=1.9; 95% CI=1.4-2.5)).

Of viral cultures (nasopharyngeal and throat swabs) obtained
from 25 ill persons, 19 grew adenovirus serotype 3. Convalescent
geometric mean titers (GMT) to adenovirus for persons with cases
during sessions one and two (GMT 14 and GMT 28, respectively) were
each significantly higher (p less than 0.01) than the GMT of
persons not meeting the case definition (GMT 6). Bacterial analysis
of grab samples of water obtained from the pond yielded 80 colonies
per 100 cc of fecal coliforms, 200 colonies per 100 cc of
enterococcus, and 9000 colonies per 100 cc of staphylococcus. A
concentrated sample of pond water drawn approximately 6 feet below
the surface yielded adenovirus serotype 3. Residual chlorine was
not detectable.

One week after the end of the second session the pond was
drained, and most counselors left. No further outbreaks were
reported following the second session; however, all subsequent
sessions during the summer and fall were of maximum 1-week
duration.

Editorial Note

Editorial Note: The illness described in this outbreak is
consistent with PCF, a syndrome caused by adenovirus (especially
serotypes 3 and 7) (1). As in previous reports (2,3), three routes
(person to person, fomites, and water contact) probably transmitted
virus in this outbreak.

Because of the turbidity of water in soil-bottom reservoirs,
chlorination is ineffective. Turbid water contains organic
molecules (e.g., humic and fulvic acids from plant decay) that
react with chlorine, generating trihalomethanes (THM), especially
chloroform (4,5); THM molecules have no antiviral activity (5).
Viruses may attach or embed in suspended particles in turbid water
(5,6), and these virus-containing particles precipitate into the
sediment on the bottom where they may remain viable in the cooler
temperatures. The virus containing particles may become resuspended
when the water is agitated by swimmers (6,7). Natural bodies of
water may have inherent virucidal properties possibly related to
certain species of bacteria (6,8). Consequently, chlorination of
natural waters may actually slow elimination of virus from the
water (6,8).

Outbreaks of both bacterial and viral diseases have been
linked to swimming in streams and reservoirs. Although North
Carolina monitors the microbiologic quality of streams and
reservoirs, it does not regulate swimming in these waters;
furthermore, there are no uniformly accepted microbiologic
standards for swimming in streams and reservoirs. Regulation of
swimming in these streams and reservoirs could be based on a
variety of parameters such as swimmer density, water turbidity, or
bacterial counts (e.g., fecal coliforms, fecal streptococcus, or
staphylococcus).

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